Brixcoyne9475
Mutation of the APC gene is not necessarily indicative of higher risk for baseline hearing loss in the pediatric population.
Clinical significance of antitumour drugs is limited by multidrug resistance (MDR). We examined the effect of bioreductive activation of the anthracyclines, doxorubicin (DOX) and pirarubicin (PIRA), by cytochrome P450 reductase (CPR) on triggering apoptosis of leukaemia HL60 cells and their MDR counterparts.
Cell cycle and FAS expression were investigated by flow cytometry. DNA fragmentation was examined by electrophoretic analysis and caspase-3/8 activities were determined colorimetrically.
Non-activated and CPR-activated forms of DOX and PIRA (IC
) had similar efficacy in provoking G
/M arrest of sensitive HL60 as well as resistant HL60/VINC and HL60/DOX cells and in causing DNA degradation. Interestingly, HL60/VINC cells were more prone to apoptosis induced by all studied forms of these drugs. However, no change in Fas expression was observed.
Bioreductive activation of DOX and PIRA does not affect their ability to induce apoptosis of sensitive and resistant HL60 leukaemia cells.
Bioreductive activation of DOX and PIRA does not affect their ability to induce apoptosis of sensitive and resistant HL60 leukaemia cells.
The current study aimed to evaluate the clinical utility of the levels of the C-X-C-motif chemokine receptor-2 (CXCR-2) serum receptor in comparison to the carcinoembryonic antigen (CEA) tumor marker and - the C-reactive protein (CRP) inflammatory marker in the diagnosis and prognosis of colorectal cancer (CRC).
Our study comprised 59 patients with CRC and 46 healthy subjects. Serum concentrations of the analyzed proteins were measured using enzyme-linked immunosorbent assay, chemiluminescent microparticle immunoassay and immunoturbidimetric methods.
Serum levels of CXCR-2 were lower, while those of CEA and CRP were significantly higher in CRC patients in comparison to the control group. The diagnostic sensitivity of CXCR-2 was higher than that of CEA, and increased when CXCR-2 analysis was combined with CEA or CRP.
According to our knowledge, this is the first study concerning the significance of CXCR2 as a CRC biomarker. mTOR inhibitor Measurement of the serum levels of CXCR-2 may improve the diagnosis efficiency of CRC patients, especially in combination with the tumor marker CEA.
According to our knowledge, this is the first study concerning the significance of CXCR2 as a CRC biomarker. Measurement of the serum levels of CXCR-2 may improve the diagnosis efficiency of CRC patients, especially in combination with the tumor marker CEA.
Recurrence and metastasis of cancer caused by cancer stem cells (CSCs) is a challenge to overcome. Low level laser therapy is a new treatment strategy to suppress their invasiveness. We have assessed the inhibitory effects of 470 nm blue LED on the invasiveness of them to determine the molecular mechanisms of anti-invasiveness.
The effects of blue LEDs on their viability, proliferation and invasion were analyzed using MTT and transwell methods. In addition, the anti-invasiveness effect of blue LED on them was evaluated by zymography, semi-quantitative RT-PCR and western blot analysis.
Irradiation with blue LED at 3 J/cm
resulted in inhibition of their viability, proliferation and invasiveness. Their matrix metalloproteinase 2 (MMP-2) and MMP-9 activities were reduced by blue LED irradiation. Semi-quantitative RT-PCR also showed similar results. In addition, western blotting analyses showed that cyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE2) synthesis were significantly inhibited by LED irradiation in CD133
colorectal CSCs.
Down-regulation of the COX-2/PGE2 signaling pathway by blue LED irradiation led to reduce expression of MMP-2 and MMP-9, inhibiting the invasiveness of CD133
colorectal CSC.
Down-regulation of the COX-2/PGE2 signaling pathway by blue LED irradiation led to reduce expression of MMP-2 and MMP-9, inhibiting the invasiveness of CD133+ colorectal CSC.
Pancreatic ductal adenocarcinoma is one of the deadliest forms of human cancer. Since only a vast panel of cell lines can fully recapitulate disease heterogeneity, our aim was to establish a new pancreatic cancer cell line.
Newly established pancreatic ductal adenocarcinoma cell line Capan-26 was characterized by assessing growth rate, tumor and stem cell marker expression, colony forming efficiency, mutations of KRAS and TP53 genes, karyotype and sensitivity to drug treatment.
Cell doubling time was 74 h. We detected CA19-9, CEACAM6, CD44, OCT4 and ZEB1 expression in Capan-26 cell line. Cells formed colonies in soft agar, have a deletion of KRAS exon 3 and a point mutation V172F in TP53 exon 5. They are a mixed aneuploid/polyploid population with high sensitivity to gemcitabine.
Capan-26 is a unique cell line that may be used to study the mechanism of pancreatic cancer.
Capan-26 is a unique cell line that may be used to study the mechanism of pancreatic cancer.
Despite clinical benefit from treatment with dabrafenib and trametinib in melanoma patients with BRAF mutations, half relapse within months and one-third are unresponsive to treatment. We evaluated the anticancer potential of metformin in combination with trametinib plus paclitaxel, against four melanoma cell lines.
Metformin with trametinib and paclitaxel was tested for effects on cell viability, signaling molecules in MAPK and mTOR pathways, factors involved in epithelial-mesenchymal transition (EMT), and cell motility.
The combination of metformin with trametinib and paclitaxel showed differential growth inhibitory effects; synergistic effects were observed in a cell line in which metformin suppresses ERK activity, whereas the combination showed antagonistic effects in a cell line with metformin-induced ERK activation. Trametinib or paclitaxel increased the expression of EMT regulators and melanoma cell motility, which were suppressed by combining metformin with trametinib and paclitaxel.
The combined treatment of metformin with trametinib and paclitaxel showed divergent effects on melanoma cell viability. Metformin might be useful as a potential adjuvant against cell proliferation and metastatic activity in melanoma patients.
The combined treatment of metformin with trametinib and paclitaxel showed divergent effects on melanoma cell viability. Metformin might be useful as a potential adjuvant against cell proliferation and metastatic activity in melanoma patients.
